Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Study of the Molecular Mechanism of Anti-inflamma-tory Activity of Bee venom in Lipopolysaccharide Stimulated RAW 264.7 Macrophages

Pham Duy Lam¹, Prabhat Kumar Mandal², Seung Yang Hak³, Seong-Gu Hwang¹

¹Division of Animal Life & Environmental Science. College of Agriculture and Life Science, Hankyong National University, Anseong-si, Gyonggi-do, S. Korea-456 749; ²Department of Food Science and Biotechnology of Animal Resources, Konkuk University, Seoul, S. Korea-143 701; ³National Institute of Animal Science, Rural Development Administration, Cheonan, S. Korea, 330-801.

For correspondence:- Seong-Gu Hwang Email: sghwang@hknu.ac.kr Tel:+82316705121

Received: 3 September 2009 Accepted: 10 November 2009 Published: 23 February 2010

Citation: Lam PD, Mandal PK, Hak SY, Hwang S. Study of the Molecular Mechanism of Anti-inflamma-tory Activity of Bee venom in Lipopolysaccharide Stimulated RAW 264.7 Macrophages. Trop J Pharm Res 2010; 9(1):19-26 doi: 10.4314/tjpr.v9i1.3

© 2010 The authors.
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Abstract

Purpose: Bee venom (BV) is traditionally used in many inflammatory chronic conditions but its mechanism of action at molecular level is not fully understood. This study was undertaken to elucidate the mechanism of action of bee venom at the molecular level.

Methods: We used lipopolysaccharide (LPS) stimulation in Raw 264.7 macrophage (RM) cells and studied the effect of BV on cell proliferation, inflammation related protein expression by western blotting and RNA expression by reverse transcriptase polymerase chain reaction (RT-PCR).

Results: Bee venom was toxic to RM cells above10 µg/ml but reduced the production of nitric oxide (NO) at 2–10 µg/ml in LPS stimulated RM cells by inhibiting the expression of inducible nitric oxide synthase (iNOS) and cyclooxigenase (COX)-2 via nuclear factor (NF)-κB. However, bee venom also induced the pro-inflammatory cytokine, interleukin (IL)-1β via p38 mitogen activated protein kinase (MAPK) which is known to stimulate inflammatory activity.

Conclusion: It seems that NFκB and p38 MAPK signal pathways are involved in triggering the functional activation of LPS-stimulated macrophage. We suggest that some components of bee venom can cause inflammation by inducing IL-1β via p38 MAPK while others act as anti-inflammatory by suppressing iNOS and COX2 via NFκB.

Keywords: Bee venom, Cyclooxygenase-2, Interleukin 1beta, Inducible nitric oxide synthase, Lipopolysaccharide, Macrophage, Mitogen activated protein kinase, Nuc